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Blood coagulation pathways in vivo showing the central role played by thrombin. Factor Xa is the activated form of the coagulation factor X, also known as thrombokinase. Factor X is an enzyme, a serine endopeptidase, which plays a key role at several stages of the coagulation system. Factor X is synthesized in the liver.
Coagulation factor concentrates are used to treat hemophilia, to reverse the effects of anticoagulants, and to treat bleeding in people with impaired coagulation factor synthesis or increased consumption. Prothrombin complex concentrate, cryoprecipitate and fresh frozen plasma are commonly used coagulation factor products.
In coagulation, the coagulation factor X can be activated into factor Xa in two ways: either extrinsically or intrinsically. The activating complexes are together called tenase. Tenase is a blend word of "ten" and the suffix "-ase", which means, that the complex activates its substrate (inactive factor X) by cleaving it. [1]
Factors VII, IX, and X all play key roles in blood coagulation and also share a common domain architecture. [10] The factor IX protein is composed of four protein domains: the Gla domain, two tandem copies of the EGF domain and a C-terminal trypsin-like peptidase domain which carries out the catalytic cleavage.
The activation of factor X is a common point between the intrinsic and extrinsic pathway of blood coagulation. [1] Activated factor X (FXa) is the sole enzyme that catalyzes the conversion of prothrombine into thrombin, which is vital in the coagulation cascade. [ 1 ]
Both factor X and factor V circulate in the blood as inactive precursors prior to activation by the coagulation cascade. The inactive zymogen factor X consists of two chains, a light chain (136 residues) and a heavy chain (306 residues).
Factor XI (FXI) is produced by the liver and circulates as a homo-dimer in its inactive form. [9] The plasma half-life of FXI is approximately 52 hours. The zymogen factor is activated into factor XIa by factor XIIa (FXIIa), thrombin, and FXIa itself; due to its activation by FXIIa, FXI is a member of the "contact pathway" (which includes HMWK, prekallikrein, factor XII, factor XI, and factor IX).
[1] [3] They may also be useful in the assessment of hypercoagulability and venous thromboembolism risk. [4] [5] [6] Levels of coagulation activation markers are increased with pregnancy, [7] with estrogen-containing birth control pills, [8] with menopausal hormone therapy, [9] [6] and with high-dose parenteral estradiol therapy for prostate ...